| Co-Investigator(Kenkyū-buntansha) |
NABETANI Akira 京都大学, 大学院生命科学研究科, 助教 (40334495)
TARUMOTO Yusuke 京都大学, 大学院生命科学研究科, 助教 (70551381)
SAKAKIBARA Yasubumi 慶應義塾大学, 理工学部, 教授 (10287427)
WAKABAYASHI Yuichi 千葉県がんセンター研究所, 発がん研究グループ, 室長 (40303119)
FUJIYOSHI Satoru 東京工業大学, 理工学研究科, 助教 (70371705)
|
|---|
| Budget Amount *help |
¥217,620,000 (Direct Cost: ¥167,400,000、Indirect Cost: ¥50,220,000)
Fiscal Year 2014: ¥43,680,000 (Direct Cost: ¥33,600,000、Indirect Cost: ¥10,080,000)
Fiscal Year 2013: ¥43,680,000 (Direct Cost: ¥33,600,000、Indirect Cost: ¥10,080,000)
Fiscal Year 2012: ¥43,680,000 (Direct Cost: ¥33,600,000、Indirect Cost: ¥10,080,000)
Fiscal Year 2011: ¥42,380,000 (Direct Cost: ¥32,600,000、Indirect Cost: ¥9,780,000)
Fiscal Year 2010: ¥44,200,000 (Direct Cost: ¥34,000,000、Indirect Cost: ¥10,200,000)
|
|---|
| Outline of Final Research Achievements |
When you get cancers, it appears that they automatically become clever: They frequently relapse after surgical resection, chemo and radiation therapy, and resist to the second line of therapies. Since we have recently witnessed outstanding advances in genetic dissection of cancer DNAs, we now need to understand molecularly how cancer cells acquire malignant phenotypes (progression). One key step of the progression is that cancer cells modify genetic materials so that it contributes to their continuous growth. In this study, we focus on telomeres, a specific domain comprising chromosomal termini. We previously isolated a protein complex called CST (Ctc1-Stn1-Ten1), which facilitates DNA replication in both normal and cancer cells. Here, we investigated details of the function of the CST complex. Results allowed us to propose how normal CST function is important for preventing cancer development and progression.
|
